Abstract
EC-coupling and Ca2+ signaling in cardiac muscle rely on Ca2+-induced Ca2+ release (CICR) from the sarcoplasmic reticulum (SR), an amplification process exhibiting a high degree of positive feed-back. To avoid instabilities of this feedback system, Ca2+ release is highly localized to elementary Ca2+ signaling events, Ca2+ sparks. The amplitude of Ca2+ transients can be modulated by recruiting fewer or more Ca2+ sparks, each of which normally remains under local control by an L-type Ca2+ channel.
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